Ventricular Tachycardia Exit Sites Research Articles

Site-specific prolongation of repolarization prevents postmyocardial infarction tachycardia.

Site-specific prolongation of repolarization prevents postmyocardial infarction tachycardia.

Ventricular tachycardia site of origin prediction by a QRS axis-based algorithm confirmed by heterogenous tissue channel localization obtained from artificial-intelligence-powered CMR analysis

Abstract Funding Acknowledgements Type of funding sources: None. Introduction A previously validated algorithm allows to accurately identify ventricular tachycardia (VT) exit site in a 17-segments American Heart Association left ventricle model in patients with structural heart disease (SHD). ADAS3D is a novel artificial-intelligence cardiac magnetic resonance (CMR) post-processing software which enables heterogeneous tissue channel (HTC) identification. Purpose The aim of this study is to compare inferred VT exit site between QRS-axis based model and HTC identification from CMR post-processing. Methods All subjects allocated to a CMR-guided or aided approach from a multicenter randomized clinical trial were analyzed. Patients with available 12-lead ECG of clinical VT obtained before ablation were analyzed in terms of concordance between VT site of origin inferred from a QRS-axis and location of HTCs in a 17-segments model. Results 10 out of 15 patients had 12-lead ECG of clinical VT (80% male, 60% with ischemic cardiomyopathy, mean age 63,5±16,95 years, mean tachycardia cycle length 373,7±99,55 ms). 7 out of 10 patients (70,00%) had at least one HTC located at VT exit site as predicted by a QRS axis-based algorithm. In all remaining cases (3 out of 10) HTC location was found in a segment adjacent to ECG-derived exit site. All patients underwent CMR-guided or CMR-aided VT ablation with acute clinical success (noninducibility of the clinical VT). Conclusion VT site of origin prediction via a QRS axis-based algorithm allows for reasonable prediction of HTC presence at inferred site of origin. Larger studies are needed in order to confirm such findings and their potential clinical implications.

Accuracy of a novel ECGi system in localising the critical isthmus exit site in scar-dependant re-entrant ventricular tachycardia

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Vision in ventricular onset (VIVO) is a novel, non-invasive, mapping system designed to locate the site of earliest activation in ventricular arrhythmia. VIVO utilises a mathematical algorithm, cross-sectional imaging data (CT or MRI), 3D images of the electrodes on the patient torso, and a 12-lead electrocardiogram (ECG) to identify the site of earliest ventricular activation.(1) The system has been shown to accurately predict earliest activation of focal premature ventricular contractions (PVCs), but its accuracy in scar dependant re-entrant ventricular tachycardia (VT) has not been investigated.(1-3) Objective To assess the accuracy of VIVO in localising the VT exit site for patients with ischaemic cardiomyopathy (ICM) and scar related re-entrant VT. Methods 5 patients with ICM (age 56 ± 19 yrs, male n = 5) were investigated (table 1). All patients had an implantable cardioverter-defibrillator with standard indications for VT ablation. Invasive electro-anatomical mapping was performed with the Advisor HD Grid multipolar catheter and maps were generated using omnipolar electrograms (EGMs). The VT exit site was identified using activation ± pace-maps and the location defined by the primary operator using the American Heart Association (AHA) 17 segment model of the left ventricle.(4) Using the intra-procedural VT ECG recordings, VIVO maps were constructed post-procedure. The VIVO predicted VT exit site was identified using the AHA 17-segment model by a second operator, blinded to the results of the procedure. A "complete match" was defined as exact segment concordance between the two operators, "partial match" as adjacent segments, and "no match" if neither requirements satisfied. Results Mean left ventricular ejection fraction was 30.5 ± 9.0%. Mean procedure time was 233 ± 31 minutes, with a mean ablation time of 24 ± 18 minutes. A total of 11 re-entrant VTs were mapped. The VT exit site was identified in all cases (10 activation-map; 1 pace-map). A complete match was seen in 91% of VTs and partial match in 9% (table 2). None of the cases demonstrated a "no match" between the invasive and VIVO maps. There were no procedural complications. Conclusion The VIVO mapping system can accurately predict the VT exit site in scar dependant re-entrant VT. Further studies to assess the feasibility of VIVO-guided ablation in scar dependant VT are ongoing.

The effect of scar imaging quality on in-silico pace-mapping of post-infarction ventricular tachycardia

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Wellcome Trust and British Heart Foundation. Background In-silico pacing mapping is a technique which involves using an anatomically-personalised image-based computational model to generate a ‘virtual’ clinical pace map for enhanced pre-procedural ablation planning of post-infarction ventricular tachycardia (VT). Utilising, as it does, a direct clinical ECG (or implanted device) recording of the clinical VT in order to construct the map, it has a number of advantages over other computational methods which attempt to simulate patient-specific VTs to identify ablation targets. However, accurate model construction relies on adequate scar imaging data, which may not be available with current clinical cardiac MR (CMR) sequences. Purpose To investigate the impact of scar imaging quality on the ability of in-silico pace-mapping to determine the VT origin. Methods VTs were simulated in three post-infarction porcine heart models reconstructed from high resolution (1mm isotropic) contrast-enhanced CMR data. Visual analysis of the VT circuits was performed to identify the VT site of origin (exit site) in each case (as the gold standard). The ECG of each simulated VT was computed and used as input for the construction of the in-silico virtual pace-mapping approach. Prior to pace map construction, the scar anatomy was modified to represent three different levels of imaging resolution: high resolution scar mapping (default); low resolution scar (representing standing clinical CMR sequences), obtained by performing dilation and erosion in the scar to close all inner pathways; and, finally, no scar (cardiac anatomy only, representing CT-based reconstructions). In-silico pace-mapping was performed by pacing the heart in N = 1000 sites from randomly chosen locations, on both surfaces and intramurally, within close proximity (<5mm) from the infarct. ECG signals computed following each paced activation wavefront were compared to the VT ECG through correlation analysis to construct the virtual pace map. The distance d between the VT exit site and the pacing location with the strongest correlation was also computed. Results As can be seen in Figure 1, correlation between VT and paced ECGs was found to be strongest at pacing locations near the VT exit site in all models. Correlation coefficients were similar in value and distribution in models with high- (min: -0.49±0.27 and max: 0.92±0.05) and low-resolution scars (min: -0.46±0.29 and max: 0.93±0.05). While the correlation map in the absence of scar had smaller values when compared to the other two models (min: -0.50±0.24 and max: 0.71±0.09), the VT exit was still located near the pacing location with the strongest correlation: d = 9.47±2.83 (high-res), d = 6.63±6.35mm (low-res) and d = 18.60±7.10mm (no scar). Conclusion In-silico pace-mapping successfully detected the VT exit sites regardless the resolution of the scar. This finding suggest that the level of infarct anatomical detail has a minor effect on simulated paced activation to localize VT ablation.

Integration of electroanatomical mapping data with whole human heart histology to identify the morphological characteristics of VT substrate in patients with NICM

Abstract Funding Acknowledgements Type of funding sources: None. Introduction The dominant mechanism of ventricular tachycardia (VT) in patients with non-ischemic cardiomyopathy (NICM) is re-entry related to fibrosis. Fibrosis in NICM is fundamentally different from post-infarct scars. Fibrosis does not equal VT substrate. The amount and characteristics of fibrosis related to VT in NICM are unknown. Aim To describe histological characteristics associated with VT substrate in patients with NICM using integration of electroanatomical mapping (EAM) data and whole human heart histology. Methods EAM data of 10 patients with NICM who died or underwent heart transplantation after catheter ablation (CA) for VT were reviewed. VT related sites were categorized as class I (entrainment response/VT termination during CA), or class II (other ablation target sites). Explanted hearts were sliced and stained. Ablation lesions were identified and excluded from histological analysis. EAM and whole heart histology were integrated and class I/II sites projected onto the slices using reversed registration and assigned to a segment (32 segment model). VT exit sites (based on 12 lead VT-ECG) were indicated on a 16-segment model (fig 1). The amount and homogeneity of fibrosis was determined. A new method to measure pattern and inhomogeneity of fibrosis was developed with scores between 0 (inhomogeneous confluent) and 0.5 (homogeneous diffuse). Results In 10 patients (9 with a class IV/V mutation) a median of 11 (range 3-18) VTs were induced. A total of 37 class I sites could be identified and 182/320 segments contained class II sites. After exclusion of ablation lesions, the LV had a median of 24.7% fibrosis (range 11.3-39.3%). Higher percentages of fibrosis were found in the basal anteroseptal ring which also contained the majority of class 1 (21/37) sites. In contrast, VT exit areas were clustered in the apico-septal and basal anterolateral segments. Class 1 VT related site segments contained more fibrosis (median 35.3% IQR [29.1-48.7] vs 22.1% [13.2-32.8], p<0.001) and were more inhomogeneous confluent (median 0.22 IQR [0.185-0.257] vs 0.27 [0.217-0.312], p=0.003) compared to segments without class 1 sites (fig 2). These findings were true for class 2 sites (p<0.004). ROC analysis determined a cut-off of >31% fibrosis for the identification of class I VT related sites (AUC: 0.75, sensitivity 72% specificity 72%). Of note, in segments with <31% fibrosis and class 1 related VT sites, there was a tendency towards inhomogeneous confluent fibrosis compared to those without VT related sites (median score 0.27 vs 0.29). Conclusion In human hearts with NICM and VT, fibrosis clusters in the basal anteroseptal ring. The majority of VT related sites are located in segments with >31% fibrosis and a higher degree of inhomogeneity but they are also found in segments with less fibrosis, but with inhomogeneous confluent fibrosis. This data suggest that location, amount and inhomogeneous confluence of fibrosis contribute to arrhythmogeneity.

Optimisation of decrementing evoked potential mapping for functional substrate identification in ischaemic ventricular tachycardia ablation

Abstract Funding Acknowledgements Type of funding sources: None. Background Decrement evoked potential (DeEP) mapping has been shown to identify the functional substrate critical to the Ventricular Tachycardia (VT) circuit with a higher specificity than late potential mapping.[1] However, there is limited data on methodological optimisation of this technique which could identify more relevant regions of conduction delay and functional block that occurs during clinical VT by activating the substrate at coupling intervals closer to the VT cycle length (CL). Purpose The goal of this study was to investigate a range of short coupled extra-stimuli and decrement thresholds to improve DeEP mapping target identification in patients with ischaemic cardiomyopathy. Methods Thirteen patients (70±12 years) underwent VT ablation. Mapping was performed with the Advisor HD Grid multipolar catheter. Maps were generated using omnipolar electrograms (EGMs). DeEP mapping was performed using 3 different extra-stimuli (S2) sequentially in each case: (1) 400 ms (DeEP-400); (2) VT cycle length (VTCL); (3) ventricular effective refractory period (VERP) + 20 ms. For each of the DeEP-400, DeEP-VTCL and DeEP-VERP maps, the definition of a DeEP was altered from the standard 10 ms decrement to multiple thresholds of 10 ms to 50 ms in 10 ms increments (figure 1). DeEP maps were compared to the VT exit site identified with VT activation maps. All patients underwent DeEP-400 focused ablation. Results All patients had 1 clinical VT (VTCL = 353 ± 48 ms; VERP + 20 ms = 300 ± 20 ms). Mean left ventricular ejection fraction was 30 ± 12 %. Sensitivity and specificity analyses (figure 2) show the optimal threshold for defining a DeEP is with an EGM prolongation of ≥ 20 ms for the DeEP-400 (sens. 77%, spec. 79%, ROC AUC 0.84), DeEP-VTCL (sens. 77%, spec. 79%, ROC AUC 0.83) and DeEP-VERP (sens. 69%, spec. 74%, ROC AUC 0.76) maps. Proportional to total mapped area, the DeEP-400 map area was significantly smaller than DeEP-VERP map area (19.0 ± 7.6 % vs 26.4 ± 14.3%; p=0.02). Delivering the S2 at the conventional VERP + 20 ms using a 10 ms decrement definition yielded a sensitivity of 84.6% and a specificity of 62.0% with a target ablation area of 33.9 cm2. With the optimised protocol of delivering the S2 at 400 ms using a 20 ms decrement definition, the sensitivity remains high at 76.9% with an improved specificity of 79.0%, thus reducing the ablation target area by 50% to 16.8 cm2. 92% patients were free of any VT after DeEP-400 guided ablation at 6-month median follow-up. Conclusion In this prospective, mechanistic study utilising omnipolar technology to explore a range of S2 extra-stimuli and decrement thresholds, DeEPs were optimally defined by a conduction delay of ≥ 20 ms with an S2 extra-stimulus coupling interval of 400 ms or VTCL to more accurately localise the VT exit site. This optimised DeEP mapping protocol further refines identification of the critical myocardial sites involved in the initiation and maintenance of VT.

PO-04-231 THERAPIES DELIVERED BEFORE AND AFTER NONINVASIVE CARDIAC RADIOABLATION: A SECONDARY ANALYSIS OF THE ENCORE-VT TRIAL

Noninvasive Cardiac RadioAblation (CRA) is a new therapy for refractory ventricular tachycardia (VT) that delivers focused radiation to VT-related myocardial scar. Because CRA reduced VT events, we hypothesize therapies will be reduced. To compare type and number of therapies delivered before and after cardiac radioablation in patients with scar-based VT. This was a retrospective analysis of ICD interrogations from the ENCORE-VT trial (NCT02919618), where patients with high-burden of VT were treated with 25 Gray/1 fraction to myocardial scar nearest the VT exit site. For each patient, all device-identified VT episodes which required therapy were reviewed for the 6-month period prior to CRA and 6-month period after (excluding 6-week blanking period). Episodes of non-sustained VT, non-treated VT, or VF were excluded. Type and number of therapies derived from device review were used for primary comparison. Of the 19 patients enrolled into the trial, 16 were included for analysis (excluded 2 patients treated for PVCs, 1 patient death in first 6 months). Cohort analysis (Top Figure) using Student’s t-test showed statistically significant reduction in VT episodes (P 0.0006) and antitachycardia pacing (ATP) therapies (P 0.0004) post therapy and a greater than 78% reduction in shocks. Compared to pre-treatment (Bottom Figure), by percentage, ATP terminated VT more often post-treatment with two or fewer sequences. Three of more ATP sequences were seen, by percentage, more often pre-treatment as compared to post-treatment. Compared to before cardiac radioablation, episodes of VT and number of therapies for VT were significantly reduced. In addition, when VT did recur post-treatment, it was more susceptible to termination by two or fewer ATP sequences.

Non-invasive localization of post-infarct ventricular tachycardia exit sites to guide ablation planning: a computational deep learning platform utilizing the 12-lead electrocardiogram and intracardiac electrograms from implanted devices.

Existing strategies that identify post-infarct ventricular tachycardia (VT) ablation target either employ invasive electrophysiological (EP) mapping or non-invasive modalities utilizing the electrocardiogram (ECG). Their success relies on localizing sites critical to the maintenance of the clinical arrhythmia, not always recorded on the 12-lead ECG. Targeting the clinical VT by utilizing electrograms (EGM) recordings stored in implanted devices may aid ablation planning, enhancing safety and speed and potentially reducing the need of VT induction. In this context, we aim to develop a non-invasive computational-deep learning (DL) platform to localize VT exit sites from surface ECGs and implanted device intracardiac EGMs. A library of ECGs and EGMs from simulated paced beats and representative post-infarct VTs was generated across five torso models. Traces were used to train DL algorithms to localize VT sites of earliest systolic activation; first tested on simulated data and then on a clinically induced VT to show applicability of our platform in clinical settings. Localization performance was estimated via localization errors (LEs) against known VT exit sites from simulations or clinical ablation targets. Surface ECGs successfully localized post-infarct VTs from simulated data with mean LE = 9.61 ± 2.61 mm across torsos. VT localization was successfully achieved from implanted device intracardiac EGMs with mean LE = 13.10 ± 2.36 mm. Finally, the clinically induced VT localization was in agreement with the clinical ablation volume. The proposed framework may be utilized for direct localization of post-infarct VTs from surface ECGs and/or implanted device EGMs, or in conjunction with efficient, patient-specific modelling, enhancing safety and speed of ablation planning.

Correlation of exit sites of inducible ventricular tachycardia post-ST elevation myocardial infarction on electrophysiology study, with region of infarct.

Ventricular arrhythmia (VA) is the most common cause of sudden cardiac death post-ST elevation myocardial infarction (STEMI). Ventricular tachycardia (VT) may be inducible in electrophysiology studies (EPS) early (<40 days) post-STEMI. Whether it originates from the infarct site remains unknown. We examined the correlation between inducible VT and infarct location post-STEMI. To investigate the correlation between inducible VT and infarct location post-STEMI. We retrospectively analysed 46 patients from 2005 to 2017 with STEMI who underwent early programmed ventricular stimulation through EPS (>48 h post-STEMI and <40 days from admission). Gated heart pool scans were used to visualise infarct scar regions, and VT exit sites were derived from induction 12-lead electrocardiography. Patients were followed up for primary outcomes of recurrent VA and all-cause mortality. Forty-six patients were included for analysis, with 50 uniquely induced VT exit sites. Mean left ventricular ejection fraction was 30 ± 8.7% and 22% had impaired right ventricular ejection fraction. Mean time from presentation to EPS was 16 ± 31.3 days. Of the induced VT, 44 (88%) were from within scar and scar-border regions, whereas 6 (12%) of the induced VT were found to be remote to imaging-derived scar. Over a median follow-up period of 75 months, 6 (13%) patients died, and 7 (15%) patients had recurrent VA. No deaths occurred in patients with remote VT. The majority of early inducible post-infarct VT arises from acute myocardial scar; however, a small portion arises from sites remote from scars with a possible focal aetiology.

In silico study of anti-tachycardia pacing efficacy optimisation through scar-targeted stimulation

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Medical Research Council, UK Background Anti-tachycardia pacing (ATP) is a reliable electrotherapy to painlessly terminate ventricular tachycardia (VT). However, ATP is often ineffective, particularly for fast VTs, which is often due to the inability of paced wavefronts to reach the re-entrant circuit, because of functional or anatomical barriers. It is thought that efficacy may be enhanced by optimised delivery closer to the re-entrant circuit driving the VT. Purpose To quantitatively assess the dependence of ATP efficacy upon different delivery locations with respect to the re-entrant circuit. Methods A cohort of 7 porcine ventricular infarct computational models were generated based on in vivo magnetic resonance imaging. Rapid-pacing protocols were applied to the cohort to induce VTs. Functional model parameters were adjusted to produce 73 episodes of sustained monomorphic VT, including 32 fast VTs (cycle length (CL)≤320ms) and 41 slow VTs (320ms-&amp;lt;VTCL≤&amp;lt;VTCL≤&amp;gt;480ms). Burst ATP (2 sequences of 8 pulses at 88% of VTCL) was separately delivered from 3 locations proximal to the re-entrant circuit (along the RV septum), specifically within the critical isthmus (CI), and at the Exit and Entrance sites, along with 3 locations distal to the circuit (lateral/posterior LV), based on multipolar implanted devices with LV epicardial leads, constituting 438 virtual scenarios and efficacy compared (Fig A). Results ATP efficacy was significantly higher for slow VTs than for fast VTs (65% vs 46%, P=0.00004) (Fig B). Separate analysis of slow VT cases revealed that delivering from distal locations to the re-entrant circuit was significantly more effective than delivering from proximal locations (72% vs 59%, P=0.04). However, for fast VT cases, the trend was reversed with proximal application (41%) being more effective than distal application (51%, P=0.15) (Fig B). Moreover, individual analysis on specific proximal locations revealed that in slow VT cases, delivering at the Exit site of VT was significantly less efficient than delivering at the Entrance site (46% vs 73%, P=0.01), with a similar (although non-significant) trend also being seen for fast VTs (44% vs 53%, P=0.5) (Fig C). Moreover, for fast VT cases, ATP delivery within the CI was overall the most effective (56%) than all other locations while this trend was not seen in slow VT cases. Conclusions ATP delivery proximal to the re-entrant circuit improves efficacy in fast VTs, but less so in slow VTs, where delivering from distal sites is superior. Specifically, for fast VTs, ATP delivery within the CI is the most effective. This work suggests that real-time alteration in applied ATP delivery site choice in a multipolar device (guided by the sensed VT rate by the device prior to therapy delivery) may be beneficial. Combined with the state-of-art leadless pacing technology, this also provides a clinical opportunity for patient-specific ATP delivery configuration and programming.

Assessment of an ECG-Based System for Localizing Ventricular Arrhythmias in Patients With Structural Heart Disease.

BackgroundWe have previously developed an intraprocedural automatic arrhythmia‐origin localization (AAOL) system to identify idiopathic ventricular arrhythmia origins in real time using a 3‐lead ECG. The objective was to assess the localization accuracy of ventricular tachycardia (VT) exit and premature ventricular contraction (PVC) origin sites in patients with structural heart disease using the AAOL system.Methods and ResultsIn retrospective and prospective case series studies, a total of 42 patients who underwent VT/PVC ablation in the setting of structural heart disease were recruited at 2 different centers. The AAOL system combines 120‐ms QRS integrals of 3 leads (III, V2, V6) with pace mapping to predict VT exit/PVC origin site and projects that site onto the patient‐specific electroanatomic mapping surface. VT exit/PVC origin sites were clinically identified by activation mapping and/or pace mapping. The localization error of the VT exit/PVC origin site was assessed by the distance between the clinically identified site and the estimated site. In the retrospective study of 19 patients with structural heart disease, the AAOL system achieved a mean localization accuracy of 6.5±2.6 mm for 25 induced VTs. In the prospective study with 23 patients, mean localization accuracy was 5.9±2.6 mm for 26 VT exit and PVC origin sites. There was no difference in mean localization error in epicardial sites compared with endocardial sites using the AAOL system (6.0 versus 5.8 mm, P=0.895).ConclusionsThe AAOL system achieved accurate localization of VT exit/PVC origin sites in patients with structural heart disease; its performance is superior to current systems, and thus, it promises to have potential clinical utility.

Computational ECG mapping and respiratory gating to optimize stereotactic ablative radiotherapy workflow for refractory ventricular tachycardia.

BackgroundStereotactic ablative radiotherapy (SAbR) is an emerging therapy for refractory ventricular tachycardia (VT). However, the current workflow is complicated, and the precision and safety in patients with significant cardiorespiratory motion and VT targets near the stomach may be suboptimal.ObjectiveWe hypothesized that automated 12-lead electrocardiogram (ECG) mapping and respiratory-gated therapy may improve the ease and precision of SAbR planning and facilitate safe radiation delivery in patients with refractory VT.MethodsConsecutive patients with refractory VT were studied at 2 hospitals. VT exit sites were localized using a 3-D computational ECG algorithm noninvasively and compared to available prior invasive mapping. Radiotherapy (25 Gy) was delivered at end-expiration when cardiac respiratory motion was ≥0.6 cm or targets were ≤2 cm from the stomach.ResultsIn 6 patients (ejection fraction 29% ± 13%), 4.2 ± 2.3 VT morphologies per patient were mapped. Overall, 7 out of 7 computational ECG mappings (100%) colocalized to the identical cardiac segment when prior invasive electrophysiology study was available. Respiratory gating was associated with smaller planning target volumes compared to nongated volumes (71 ± 7 vs 153 ± 35 cc, P < .01). In 2 patients with inferior wall VT targets close to the stomach (6 mm proximity) or significant respiratory motion (22 mm excursion), no GI complications were observed at 9- and 12-month follow-up. Implantable cardioverter-defibrillator shocks decreased from 23 ± 12 shocks/patient to 0.67 ± 1.0 (P < .001) post-SAbR at 6.0 ± 4.9 months follow-up.ConclusionsA workflow including computational ECG mapping and protocol-guided respiratory gating is feasible, is safe, and may improve the ease of SAbR planning. Studies to validate this workflow in larger populations are required.

B-PO01-090 PROSPECTIVE ASSESSMENT OF AN AUTOMATED INTRAPROCEDURAL ECG-BASED SYSTEM FOR LOCALIZING VT EXIT SITES IN PATIENTS WITH STRUCTURAL HEART DISEASE (SHD)

We have previously developed an intraprocedural automatic arrhythmia origin localization (AAOL) system to localize idiopathic ventricular arrhythmia origins onto patient-specific electroanatomic (EAM) surface in real time using a 3-lead ECG. To assess the localization accuracy of ventricular tachycardia (VT) exit and premature ventricular complex (PVC) origin sites in patients with SHD using the AAOL system. In retrospective and prospective cohorts, a total of 42 patients who underwent VT/PVC ablation in the setting of SHD were recruited at two different centers. The AAOL system combines 120-ms QRS integrals of 3 leads (III, V2, V6) with pace mapping to predict VT exit/PVC origin site and projects that site onto the patient-specific electroanatomic surface. VT exit/PVC origin sites were clinically identified by contact mapping. The localization error of the VT exit/PVC origin site was assessed by the distance between the clinically identified site and the estimated site. In the retrospective cohort of 19 patients with SHD, the AAOL system achieved a mean localization accuracy of 6.5±2.6mm for 25 induced VTs. In the prospective cohort with 23 patients, mean localization accuracy was 5.9±2.6mm for 26 VT exit and PVC origin sites (Figure 1). There was no difference in mean localization error in epicardial sites compared to endocardial sites using the AAOL system (6.0 vs. 5.8 mm, P =0.895). Figure 1 shows an example of VT exit site localization. The AAOL system achieved accurate localization of VT exit/PVC origin sites in patients with SHD that is superior to current system, which supports the potential clinical utility.

Management of ventricular tachycardia in patients with cardiac sarcoidosis.

Sarcoidosis is a multisystem granulomatous disease with 2 different phases (inflammation and scar). In the current era of targeted use of implantable cardioverter-defibrillators and modern heart failure therapy, recent data indicate the prognosis of cardiac sarcoidosis (CS) is much improved, and hence more patients are presenting with recurrent ventricular tachycardia (VT). This review highlights our current understanding of the pathophysiology and management of ventricular arrhythmias in CS with the major focus on indications, techniques, and outcomes of ablation.It is likely macroreentry phenomena around areas of fibrosis is the most frequent mechanism of ventricular arrhythmia in CS. It is also possible that inflammation may play a role in initiating reentry with ventricular ectopy in CS patients, or by slowing conduction in diseased tissue. The best available data would suggest annual rates of VT of perhaps 1%–2% and 10%–15% in patients with initially clinically silent and clinically manifest disease, respectively. Current guidelines recommend a stepwise approach to VT management. The first suggested step is treatment with immunosuppression if there is evidence of active inflammation. Antiarrhythmic medications are often started at the same time, with catheter ablation considered if VT cannot be controlled. Activation and entrainment mapping and ablation are favored in the setting of hemodynamically tolerated VT. Substrate ablation targets areas of abnormal electrogram and favorable pace mapping using linear and/or cluster lesion sets with the goal of abolishing critical isthmuses and/or blocking VT exit sites. Epicardial mapping ablation is required in 20%–35% of cases. In general, more morphologies of VT are induced (often 3–4) and subsequent outcomes (recurrence rates 40%–50%) are less favorable than in other forms of nonischemic cardiomyopathy.The prognosis of CS is much improved and, as a result, more patients are developing VT during follow-up. Likely principally related to the complex disease substrate, VT ablation is technically challenging, with moderate outcomes, and much remains to be learned.

Metabolic Scar Assessment with18F-FDG PET: Correlation to Ischemic Ventricular Tachycardia Substrate and Successful Ablation Sites.

The functional and molecular imaging characteristics of ischemic ventricular tachycardia (VT) substrate are incompletely understood. Our objective was to compare regional 18F-FDG PET tracer uptake with detailed electroanatomic maps (EAMs) in a more extensive series of postinfarction VT patients to define the metabolic properties of VT substrate and successful ablation sites. Methods: Three-dimensional (3D) metabolic left ventricular reconstructions were created from perfusion-normalized 18F-FDG PET images in consecutive patients undergoing VT ablation. PET defects were classified as severe (defined as <50% uptake) or moderate (defined as 50%-70% uptake), as referenced to the maximal 17-segment uptake. Color-coded PET scar reconstructions were coregistered with corresponding high-resolution 3D EAMs, which were classified as indicating dense scarring (defined as voltage < 0.5 mV), normal myocardium (defined as voltage > 1.5 mV), or border zones (defined as voltage of 0.5-1.5 mV). Results: All 56 patients had ischemic cardiomyopathy (ejection fraction, 29% ± 12%). Severe PET defects were larger than dense scarring, at 63.0 ± 48.4 cm2 versus 13.8 ± 33.1 cm2 (P < 0.001). Similarly, moderate/severe PET defects (≤70%) were larger than areas with abnormal voltage (≤1.5 mV) measuring 105.1 ± 67.2 cm2 versus 56.2 ± 62.6 cm2 (P < 0.001). Analysis of bipolar voltage (23,389 mapping points) showed decreased voltage among severe PET defects (n = 10,364; 0.5 ± 0.3 mV) and moderate PET defects (n = 5,243; 1.5 ± 0.9 mV, P < 0.01), with normal voltage among normal PET areas (>70% uptake) (n = 7,782, 3.2 ± 1.3 mV, P < 0.001). Eighty-eight percent of VT channel or exit sites (n = 44) were metabolically abnormal (severe PET defect, 78%; moderate PET defect, 10%), whereas 12% (n = 6) were in PET-normal areas. Metabolic channels (n = 26) existed in 45% (n = 25) of patients, with an average length and width of 17.6 ± 12.5 mm and 10.3 ± 4.2 mm, respectively. Metabolic channels were oriented predominantly in the apex or base (86%), harboring VT channel or exit sites in 31%. Metabolic rapid-transition areas (>50% change in 18F-FDG tracer uptake/15 mm) were detected in 59% of cases (n = 33), colocalizing to VT channels or exit sites (15%) or near these sites (85%, 12.8 ± 8.5 mm). Metabolism-voltage mismatches in which there was a severe PET defect but voltage indicating normal myocardium were seen in 21% of patients (n = 12), 41% of whom were harboring VT channel or exit sites. Conclusion: Abnormal 18F-FDG uptake categories could be detected using incremental 3D step-up reconstructions. They predicted decreasing bipolar voltages and VT channel or exit sites in about 90% of cases. Additionally, functional imaging allowed detection of novel molecular tissue characteristics within the ischemic VT substrate such as metabolic channels, rapid-transition areas, and metabolism-voltage mismatches demonstrating intrasubstrate heterogeneity and providing possible targets for imaging-guided ablation.

Abstract 16347: Simplified Workflow to Improve the Precision of Non-invasive Radio-ablation of Ventricular Tachycardia Storm

Background: Stereotactic ablative radiotherapy (SAbR) is an emerging therapy for ventricular tachycardia (VT) storm, but the feasibility and outcomes guided by computational 12-lead ECG mapping and respiratory-gated radiation delivery have not been reported. Hypothesis: We hypothesized that a novel 12-lead ECG-based mapping system and respiratory-gated radiotherapy delivery may simplify the workflow and improve precision of SAbR in critically ill patients with VT storm. Methods: We enrolled patients with VT storm who were not candidates for catheter ablation. VT was induced using non-invasive stimulation and recorded on 12-lead ECGs. Computational ECG mapping was performed to localize VT exit sites. Target volumes were contoured onto an averaged free-breathing CT. Ionizing radiation (25 Gy) was delivered using a linear accelerator (Varian, Palo Alto). In patients with significant respiratory motion, radiotherapy was delivered at end-expiration, guided by ICD lead fiducials. Results: In 5 patients (age 74±6.1 years, EF 29±14%) refractory to 2±1 ablation procedures, 1.5±0.6 VT morphologies were localized on 3D models (Fig 1A) using ECG-based mapping (mapping time 1.2±0.3 min). In patients whom respiratory gating (Fig 1B) was used prospectively due to respiratory variation, the planned target volume (PTV) was smaller compared to patients who were not gated (71 ± 7 vs 153 ± 35 cc, p&lt;0.01). These patients also had VT targets (crux or inferior LV) close to the stomach, and did not experience adverse events. ICD shocks were decreased after SAbR compared to before (0.25±0.5 vs 26±19 shocks, p&lt;0.001) at 4.4±3.4 months follow-up. Conclusion: Non-invasive computational mapping based upon the 12-lead ECG alone simplifies radioablation workflow in critically ill VT storm patients and reduces the burden of ICD shocks. Respiratory gated radiotherapy ablation appears feasible and may help reduce target volume of therapy. Studies with longer follow-up are ongoing.

Abstract 12974: Successful VT Ablation Utilising Intracoronary Gelatin Sponge Injection

Introduction: We report two cases of recurrent ventricular tachycardia (VT) successfully treated by intra-coronary Gelatin sponge embolization where initial endocardial ablation was unsuccessful and epicardial approaches were unfavourable. Case Histories: (1) A 75-year-old male with Inferior STEMI who underwent PCI to oRPDA developed VT storm that required DCCV 11 times. The VT was hemodynamically unstable, hence only substrate modification was performed. He still had recurrent episodes of VT and a second ablation attempt localised VT circuit breakout to the infero-apical septum, but ablation was unsuccessful due to a deep intramural circuit. Epicardial ablation was not attempted due to a 1cm pericardial effusion after the first procedure. Unipolar signals from selective wiring of the distal rPDA with a percutaneous coronary intervention guidewire and microcatheter showed early local electrograms. 5ml of Gelatin sponge injection was injected after a 5x2mm coil failed to occlude the distal rPDA. Post occlusion, VT was not inducible with double ventricular extra-stimuli. He has been VT free for 5 months (2) A 41-year-old female with dilated cardiomyopathy, previous left ventricular assist device and revision was admitted for VT storm. The VT map identified earliest activation with far-field pre-systolic potentials at the baso-lateral LV segment. Pre-systolic far field ventricular EGMs were also seen in the adjacent coronary sinus, consistent with a likely epicardial exit site of the VT. Endocardial ablation failed, and epicardial access was not feasible due to adhesions. Coronary angiography revealed a small calibre non dominant left circumflex artery supplying the VT exit site. Cold saline injection down the mLCX terminated the VT and the vessel was occluded with 5 ml of Gelatin sponge. VT was subsequently not inducible. Discussion &amp; Conclusion: Critical portions of VT circuits may course epicardially or intramurally 3 , limiting successful endocardial catheter ablation. Epicardial access was risky. Coronary vessel embolization using coils 4 and ethanol 5 have been performed. Use of absorbable Gelatin sponge has been described in managing coronary perforation 6 , but to the best of our knowledge these are the first cases of its use in VT ablation.

Association of septal late gadolinium enhancement on cardiac magnetic resonance with ventricular tachycardia ablation targets in nonischemic cardiomyopathy

Ablation of septal substrate-associated ventricular tachycardia (VT) in patients with nonischemic cardiomyopathy (NICM) is challenging. We sought to standardize the characterization of septal substrates on late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) and to examine the association of that substrate with VT exit and isthmus sites on invasive mapping. LGE-CMR was performed before electroanatomic mappingand ablation for VT in 20 NICM patients. LGE extent and distribution were quantified using myocardial signal-intensity Z scores (SI-Z). The SI-Z thresholds correlating to previously validated voltage thresholds, for abnormal tissue and dense scar were defined. Bipolar and unipolar (electrogram) voltage amplitude measurements from the LV and RV were negatively associated with SI-Z from LGE-CMR imaging (p < .05). SI-Z thresholds for appropriate CMR identification of septal substrates were determined to be greater than-.15 for border zone and greater than .03 for a dense scar. Among all patients, 34 critical VT sites were identified with SI-Z distribution in the range of -.97 to .06. Thirty (88.2%) critical sites were located in the dense LGE, 1 (2.9%) in the border zone, and 3 (8.9%) in healthy tissue but within 7 mm of LGE. Of note, critical VT sites were all located at the basal septum close to valves (distance to aortic valve: 17.5 ± 31.2 mm, mitral valve: 21.2 ± 8.7 mm) in nonsarcoidosis cases. Critical sites of septal VT in NICM patients are predominantly in the CMR defined dense scar when using standardized signal-intensity thresholds.

Initial Experience with High-density Mapping of Ischemic Ventricular Tachycardia Using a Narrow 0.1-mV to 0.25-mV Border-zone Window.

This study sought to determine (1) whether the use of a narrow border-zone voltage of 0.1 to 0.25 mV predicts the ventricular tachycardia (VT) exit site better than when using the conventional 0.5 to 1.5 mV window and (2) the feasibility of utilizing the Rhythmia mapping system (Boston Scientific, Natick, MA, USA) to map hemodynamically unstable VT without hemodynamic support. The Ablation of ischemic VT is challenging especially in the setting of hemodynamic instability, yet efficient and accurate mapping of VT and VT substrate is critical for procedural success. In this study, a total of 24 patients with ischemic cardiomyopathy and recurrent monomorphic VT underwent mapping and ablation using the Rhythmia system. Contact-force sensing ablation catheters were use in two cases. In patients with mappable VTs, the distance between the exit site and border zone was calculated for border zone-voltage windows of 0.5 to 1.5 mV and 0.1 to 0.25 mV. The percentage of LV scar for each patient was visually estimated into quartiles of scar burden in both windows. Twenty patients were inducible into VT, while 15 patients had mappable VTs for a total of 16 VTs (11 stable VTs and five unstable VTs). There were no adverse complications in patients who underwent mapping in unstable VT. The mean distance from the VT exit site to the border zone was 13.3 mm in the conventional window and 3.4 mm in the narrow window (95% confidence interval: 4.0–15.8; p = 0.003). Separately, 94% (15/16) of the VTs were mapped to the narrow border-zone voltage versus 31% (5/16) using the conventional border zone (p = 0.0006). The use of a narrow 0.1- to 0.25-mV border-zone window highlights relevant scar and constitutes a border zone where VT exit sites are frequently located. We also found that exit sites of hemodynamically unstable VTs can be identified without an increase in procedural complications using the Orion catheter (Boston Scientific, Natick, MA, USA).

In-silico pace-mapping using a detailed whole torso model and implanted electronic device electrograms for more efficient ablation planning

BackgroundPace-mapping is a commonly used electrophysiological (EP) procedure which aims to identify exit sites of ventricular tachycardia (VT) by matching ventricular activation patterns (assessed by QRS morphology) at specific pacing locations with activation during VT. However, long procedure durations and the need for VT induction render this technique non-optimal.To demonstrate the potential of in-silico pace-mapping, using stored electrogram (EGM) recordings of clinical VT from implanted devices to guide pre-procedural ablation planning. MethodSix scar-related VT episodes were simulated in a 3D torso model reconstructed from computed tomography (CT) imaging data, including three different infarct anatomies mapped from infarcted porcine imaging data. In-silico pace-mapping was performed to localise VT exit sites and isthmuses by using 12-lead electrocardiogram (ECG) signals and different combinations of EGM sensing vectors from implanted devices, through the creation of conventional correlation maps and reference-less maps. ResultsOur in-silico platform was successful in identifying VT exit sites for a variety of different VT morphologies from both ECG correlation maps and corresponding EGM maps, with the latter dependent upon the number of sensing vectors used. We also showed the added utility of both ECG and EGM reference-less pace-mapping for the identification of slow-conducting isthmuses, uncovering the optimal algorithm parameters. Finally, EGM-based pace-mapping was shown to be more dependent upon the mapped surface (epicardial/endocardial), relative to the VT origin. ConclusionsIn-silico pace-mapping can be used along with EGMs from implanted devices to localise VT ablation targets in pre-procedural planning.